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I. Intensive care


  1. Apnea and bradycardia

    1. Definition

      1. Apnea of infancy is traditionally defined as the absence of breathing for 20 seconds or longer, or a shorter respiratory pause associated with bradycardia, cyanosis, pallor, and/or marked hypotonia.

      2. The term apnea of prematurity generally refers to infants with gestational age of less than 37 weeks at the onset of apnea.

      3. Apnea is further divided into central apnea (no respiratory effort), obstructive apnea (infant initiates breath but no airflow), and mixed apnea (central and obstructive, most common type in older preterm infants).

      4. The definition of bradycardia should change in relationship to both gestational age and postconceptional age (PCA).

      5. There is no standard definition for a significant cardiorespiratory event in preterm infants.

    2. Incidence

      1. Apnea and bradycardia are common problems that have plagued neonatologists for decades, primarily in high-risk preterm infants.

      2. The problem may be more prevalent today than before the mid-1990s, given the increasing numbers of physiologically immature infants on less invasive forms of respiratory support (continuous positive airway pressure [CPAP], high-flow nasal cannula, and nasal intermittent positive pressure ventilation).

    3. Pathophysiology

      1. Immature respiratory system (Figure 8-1)

        • In the vast majority of otherwise healthy preterm infants who exhibit various combinations of central and obstructive apnea, bradycardia, and desaturation, the underlying problem is immature respiratory control.

        • Physiologic studies in both infants and immature animal models have demonstrated impaired ventilatory responses to hypercapnia, either decreased or increased hypoxic responses, exaggerated inhibitory responses to stimulation of airway (eg, laryngeal) receptors, and presumably an immaturity in the way these afferent pathways are integrated in the preterm brainstem.

        • Given that fetal breathing movements are only intermittent, function primarily to promote lung growth, and play no role in gas exchange, it is not surprising that postnatal respiratory activity is also often irregular in preterm infants.

      2. Hypercapnia

        • Hypercapnia is the major chemical driver of ventilation and sensed primarily centrally by chemosensitive cells in the brainstem that respond to either H+, CO2, or both.

        • The impairment of central chemosensitivity in preterm neonates is evident by a diminished ventilatory response to CO2 when compared to term neonates or adults. This impairment of hypercapnic ventilatory responses is also more pronounced in preterm neonates with apnea when compared to their controls without apnea.

        • Baseline PaCO2 in both preterm and term infants is only 1 to 2 mm Hg above the apneic threshold, and the contribution of closeness of the apneic threshold to baseline CO2, together with excessive activation of the carotid body, might be an unstable combination that allows small oscillations of CO2 in response to mild hyperventilation to cause apnea.

      3. Hypoxia

        • The peripheral chemoreceptors are located primarily in the carotid body and are responsible for stimulating breathing in response to hypoxia.

        • It is reasonable to assume that these chemoreceptors contribute to resolution of apnea and, if silenced (eg, by hyperoxic exposure), it may lead to prolongation of apnea.

        • After an initial excitation of breathing, preterm infants respond ...

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